Estimation of left-ventricular systolic performance and its determinants in man from pressures and dimensions of one beat: effects of aortic valve stenosis and replacement.
Within a thick heart-chamber wall, there is a midwall element or layer whose displacements best express systolic performance. The volume enclosed by that midwall element (Vm) and the average stress in that element (sigma m) can be calculated accurately by simple formulae. From simultaneous left-side pressure tracings and contrast cine-ventriculograms, Vm and sigma m were calculated at 20-ms intervals for an entire cardiac cycle in five normal subjects and in eight patients before and one year after replacement of stenotic aortic valves. Prior to surgery, the overloaded left ventricles were not hypertrophied enough to restore normal mid- and end-ejection stresses. Four had subnormal cavity ejection fractions, but all had subnormal midwall ejection fractions. All had subnormal fractional midwall ejection rates and prolonged active intervals (from the beginning of activation to the end of deactivation). Judging from pre-ejection pressure-development rates, the pressure-developing ability was not consistently elevated by concentric hypertrophy, because the stress-developing ability (contractility) was usually subnormal. The ability to shorten in the absence of afterload appeared to be subnormal in about half of the cases. The subnormal midwall ejection fractions appeared to be due to various combinations of increased mid- and late-ejection stresses, reduced contractility, and reduced shortening ability. On average and in several cases, reduced shortening ability appeared to be the main cause of the reduced performance. The effect of the slowed fractional midwall ejection rate to reduce the midwall ejection fraction was partially compensated by a prolonged active interval, by prolonged ejection time relative to the active interval, and by a more sustained ejection rate. Valve replacement partially restored all values except contractility towards normal, but the restorations of wall/cavity ratio and active interval were slight.
Regen
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Department of Molecular Physiology and Biophysics, Vanderbilt University Medical School, Nashville, TN 37232.
Nonogi
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Hess
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OM
D000328:Adult; D001021:Aortic Valve; D001024:Aortic Valve Stenosis / Q000503:physiopathology* / Q000601:surgery; D002932:Cineangiography; D006350:Heart Valve Prosthesis; D006801:Humans; D008875:Middle Aged; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology*